Protective Effect of Ganoderma atrum Polysaccharide on Acrolein-Induced Apoptosis and Autophagic Flux in IEC-6 Cells

• Published in: Foods Vol. 11; no. 2; p. 240
• Main Authors: Wang, Yudan, Chang, Xinxin, Zheng, Bing, Chen, Yi, Xie, Jianhua, Shan, Jialuo, Hu, Xiaoyi, Ding, Xiaomeng, Hu, Xiaobo, Yu, Qiang
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 17.01.2022; MDPI
• Subjects: Acrolein; AKT protein; Apoptosis; aspartic acid; Autophagy; B-cell lymphoma; Bcl-2 protein; Biotechnology; Caspase-9; Cell culture; Cell viability; cysteine; Food; Food science; Ganoderma; IEC-6 cells; Inhibitors; Kinases; Laboratories; Lymphocytes B; Lymphoma; mammals; Membrane potential; Microtubule-associated proteins; Mitochondria; mitochondrial membrane; Oxidative stress; polysaccharide; Polysaccharides; protective effect; Proteins; Rapamycin; Signal transduction; Statistical analysis; tight junctions; TOR protein; Variance analysis; Beijing China; United States > US; China; apoptosis; autophagy; polysaccharide; IEC-6 cells; acrolein
• ISSN: 2304-8158; 2304-8158
• DOI: 10.3390/foods11020240

This study was designed to explore the beneficial effect and mechanism of Ganoderma atrum (G. atrum) polysaccharide (PSG-1) on acrolein-induced IEC-6 cells. Our results indicated that PSG-1 significantly reduced the impairment of acrolein on cell viability, decreased oxidative stress, and enabled normal expression of tight junction (TJ) proteins that were inhibited by acrolein in IEC-6 cells. Furthermore, PSG-1 attenuated the elevation of microtubule-associated proteins light chain 3 (LC3) and Beclin 1-like protein 1 (Beclin 1) and increased the protein levels of phospho-mTOR (p-mTOR) and phospho-akt (p-akt), indicating that PSG-1 activated the mammalian target of rapamycin (mTOR) signaling pathway and alleviated acrolein-induced autophagy in IEC-6 cells. Moreover, PSG-1 markedly attenuated the acrolein-induced apoptosis, as evidenced by the increase in mitochondrial membrane potential (MMP) and B-cell lymphoma 2 (Bcl-2) expression, and the decrease in cysteine aspartate lyase (caspase)-3 and caspase-9. In addition, autophagy the inhibitor inhibited acrolein-induced TJ and apoptosis of IEC-6 cells, while the apoptosis inhibitor also inhibited acrolein-induced TJ and autophagy, suggesting that autophagy and apoptosis were mutually regulated. Taken together, the present study proved that PSG-1 could protect IEC-6 cells from acrolein-induced oxidative stress and could repair TJ by inhibiting apoptosis and autophagic flux, where autophagy and apoptosis were mutually regulated.